Sur la cristallinité des biotites kaolinitisées des sols ferrallitiques de la région d'Ambalavao (Madagascar)

Cet article présente une étude minéralogique des "kaolinites" des sols ferrallitiques de la région d'Ambalavao. Suite aux analyses effectuées, les auteurs montrent qu'il s'agit de kaolinites désordonnées et de composés amorphes de même composition chimique. Ils supposent que l'abaissement d'enthalpie libre de formation de ces composés amorphes par rapport à celle de la kaolinite pourrait être à l'origine de leur transformation en gibbsite même en présence de quart

Very Few RNA and DNA Sequence Differences in the Human Transcriptome

RNA editing is an important cellular process by which the nucleotides in a mature RNA transcript are altered to cause them to differ from the corresponding DNA sequence. While this process yields essential transcripts in humans and other organisms, it is believed to occur at a relatively small number of loci. The rarity of RNA editing has been challenged by a recent comparison of human RNA and DNA sequence data from 27 individuals, which revealed that over 10,000 human exonic sites appear to exhibit RNA-DNA differences (RDDs). Many of these differences could not have been caused by either of the two previously known human RNA editing mechanisms—ADAR-mediated A→G substitutions or APOBEC1-mediated C→U switches—suggesting that a previously unknown mechanism of RNA editing may be active in humans. Here, we reanalyze these data and demonstrate that genomic sequences exist in these same individuals or in the human genome that match the majority of RDDs. Our results suggest that the majority of these RDD events were observed due to accurate transcription of sequences paralogous to the apparently edited gene but differing at the edited site. In light of our results it seems prudent to conclude that if indeed an unknown mechanism is causing RDD events in humans, such events occur at a much lower frequency than originally proposed

Immunohistochemical analysis of NaPi2b protein (MX35 antigen) expression and subcellular localization in human normal and cancer tissues

Aim: To study the expression profile of the NaPi2b protein and its localization in breast, ovarian and lung cancer cells in relation to normal tissues adjacent to tumor. Methods: Immunohistochemical analysis with monoclonal antibody MX35 was applied for investigation of NaPi2b protein expression in breast, lung and ovarian carcinomas. Intensity of NaPi2b protein expression was calculated with semiquantitative scores. Results: NaPi2b (MX35) protein expression was detected in breast, lung and ovarian cancer cells and adjacent normal tissue. We have shown that in contrast to ovarian tumors in breast and lung tumors NaPi2b expression is down regulated comparing to correspondent normal tissues. Conclusion: This study provides the data on the pattern of NaPi2b expression and cellular localization in breast, lung and ovarian cancers, which might be useful for understanding the mechanism of transport and maintenance of inorganic phosphate in cancer and normal cells, as well as for developing novel immunotherapeutic approaches based on MX35 monoclonal antibody

Stat2 loss disrupts damage signalling and is protective in acute pancreatitis

The severity of sterile inflammation, as seen in acute pancreatitis, is determined by damage-sensing receptors, signalling cascades and cytokine production. Stat2 is a type I interferon signalling mediator that also has interferon-independent roles in murine lipopolysaccharide-induced NF-κB-mediated sepsis. However, its role in sterile inflammation is unknown. We hypothesised that Stat2 determines the severity of non-infective inflammation in the pancreas. Wild type (WT) and Stat2-/- mice were injected intraperitoneally with caerulein or L-arginine. Specific cytokine-blocking antibodies were used in some experiments. Pancreata and blood were harvested 1 h and 24 h after the final dose of caerulein and up to 96 h post L-arginine. Whole-tissue phosphoproteomic changes were assessed using label-free mass spectrometry. Tissue-specific Stat2 effects were studied in WT/Stat2-/- bone-marrow chimera and using Cre-lox recombination to delete Stat2 in pancreatic and duodenal homeobox 1(Pdx1)-expressing cells. Stat2-/- mice were protected from caerulein- and L-arginine-induced pancreatitis. Protection was independent of type I interferon signalling. Stat2-/- mice had lower cytokine levels including TNFα and IL-10 and reduced NF-kB nuclear localisation in pancreatic tissue compared to WT. Inhibition of TNFα improved (inhibition of IL-10 worsened) caerulein-induced pancreatitis in WT but not Stat2-/- mice. Phosphoproteomics showed down-regulation of mitogen-activated protein kinase (MAPK) mediators but accumulation of Ser412-phosphorylated Tak1. Stat2 deletion in Pdx1-expressing acinar cells (Stat2flox/Pdx1-cre ) reduced pancreatic TNFα expression, but not histological injury or serum amylase. WT/Stat2-/- bone-marrow chimera mice were protected from pancreatitis irrespective of host or recipient genotype. Stat2 loss results in disrupted signalling in pancreatitis, upstream of NF-κB in non-acinar and/or bone marrow derived cells. This article is protected by copyright. All rights reserved

Application of serex-analysis for identification of human colon cancer antigens

Copyright © Experimental Oncology, 2015. Background: Colorectal, lung and breast tumors are the most devastating and frequent malignances in clinical oncology. SEREX-analysis of colon cancer leads to identification of more than hundred antigens which are potential tumor markers. With idea that immunoscreening with pool of allogeneic sera is more productive for antigen isolation, SEREX-analysis was applied to four cases of stages II-IV primary colon tumor and 22 new antigens were isolated. Objective: To characterize 22 primary colon cancer antigens isolated by SEREXtechnique. Materials and Methods: Allogenic screening, real-time PCR analysis. Results: After allogeneic immunoscreening, for 5 of 22 (22%) isolated antigens were confirmed colon cancer restricted serological profile solely positive for 14% of tested colon cancer sera. Through these five antigens, KY-CC-17/β-actin has cytoskeleton function; KY-CC-14/ACTR1A and KY-CC-19/TSGA2 participate in chromosome segregation; KY-CC-12/FKBP4 regulates steroid receptor function and KY-CC-15/PLRG1 is a component of spliceosome complex. For the last four antigens tested were found aberrant mRNA expression in some cases of colon tumor. Conclusion: The exploration of identified antigens may define suitable targets for immunotherapy or diagnostic of colon cancer

The TSC1-2 tumor suppressor controls insulin–PI3K signaling via regulation of IRS proteins

Insulin-like growth factors elicit many responses through activation of phosphoinositide 3-OH kinase (PI3K). The tuberous sclerosis complex (TSC1-2) suppresses cell growth by negatively regulating a protein kinase, p70S6K (S6K1), which generally requires PI3K signals for its activation. Here, we show that TSC1-2 is required for insulin signaling to PI3K. TSC1-2 maintains insulin signaling to PI3K by restraining the activity of S6K, which when activated inactivates insulin receptor substrate (IRS) function, via repression of IRS-1 gene expression and via direct phosphorylation of IRS-1. Our results argue that the low malignant potential of tumors arising from TSC1-2 dysfunction may be explained by the failure of TSC mutant cells to activate PI3K and its downstream effectors